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CDC HIV/AIDS/Viral Hepatitis/STD/TB Prevention News Update
UNITED KINGDOM; UNITED STATES: Insights into How TB Tricks the Immune System Could Help Combat the Disease
Staff Writer
October 24, 2013
Medical Xpress (10.23.2013) Aids Weekly Plus

TB bacteria cause persistent TB infection by living in macrophages, the immune system cells that usually destroy invading microorganisms. Researchers from Imperial College London and California’s Stanford University have discovered how unusual sugars on the surface of the TB mycobacteria help them fasten onto the macrophages and prevent the macrophages from attacking. The researchers hope that this discovery can help in developing small molecule drugs that attach to the same site and fight TB. The drugs could function by creating a barrier to prevent the mycobacteria from attaching to the macrophages, transporting drugs to kill the mycobacteria, or changing the macrophages’ behavior and causing them to destroy the mycobacteria. Kurt Drickamer, professor at the Department of Life Sciences at Imperial College London and the study’s lead author, commented that the researchers were surprised to find an extensive interaction between the macrophage and a specific type of molecule on the surface of the mycobacteria. The researchers believe they could use the new insights into how macrophages can be switched on and off to provide better vaccines against many diseases. Although animal vaccines use mycobacteria to attract macrophages, this method was considered to be too toxic for human use. Dr. Maureen Taylor, also from Imperial College London’s Department of Life Sciences and co-author of the research, noted that scientists might be able to use the new, simpler molecules described in the research to overcome the problem of creating an immune system response to develop vaccines against many diseases. The full report, “Mechanism for Recognition of an Unusual Mycobacterial Glycolipid by the Macrophage Receptor Mincle,”was published in the Journal of Biological Chemistry (2013; 288(40):28457–65).